Team
| Nachname | Vorname | Titel | Fon | Fax | Raum/Labor | Gebäude | Funktion | ||
| Cirstea | Ion Cristian | Dr. | CV | 23889 | 36202 | ion.cirstea(at)uni-ulm.de | 3.30 | N26 | Gruppenleiter |
| Engler | Melanie | Dr. | 23889 | 36202 | melanie.engler(at)uni-ulm.de | 3.30 | N26 | Postdoc | |
| Ireri | Moses Munene | M.Sc. | 23889 | 36202 | moses.ireri(at)uni-ulm.de | 3.30 | N26 | Doktorand |
Forschungsfokus
Cirstea Research Group focuses on the identification of novel RAS-controlled biological processes and -signaling pathways that are implicated in cancer, RASopathies and neuronal development, energy metabolism, and premature aging and aging-related diseases. For our research, we use cellular and mouse models and a wide variety of cell-based and biochemical techniques.
Most important research directions:
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Novel treatment strategies in neurodevelopmental RASopathies
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Non-canonical functions of RAS GTPases in RASopathies-associated pathologies e.g., energy metabolism, bone homeostasis, and premature aging ang aging-related disorders
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Novel regulators of RAS function in cancer, RASopathies and other diseases
- The functional cross-talk between RAS and its killer protein LZTR1 in Noonan syndrome, cancer and aging. https://doi.org/10.1093/hmg/ddy412.
- The RAS GTPases and glucocorticoid receptor cross-talk in cancer. https://doi.org/10.1126/scisignal.abm4452; https://doi.org/10.1016/j.tcb.2022.11.002.
- EGFR-RAS-MAPK functional cross-talk with ACE2 in viral infection and other diseases. https://doi.org/10.26508/lsa.202201880
EURAS
Ausgewählte Publikationen
Engler M, Albers D, Von Maltitz P, Groß R, Münch J, Cirstea IC. ACE2-EGFR-MAPK signaling contributes to SARS-CoV-2 infection. Life Sci. Alliance 2023, 6(9):e202201880.
Cirstea IC*#, Moll HP*#, Tuckermann J*#. Glucocorticoid receptor-RAS - an unexpected couple in cancer. Trends in Cell Biology. 2023, S0962-8924(22)00253-7. *#, Equal contribution and correspondence
Nandi S, Chennappan S, Andrasch Y, Fidan M, Engler M, Ahmad M, Tuckermann JP, Zenker M, Cirstea IC. Increased osteoclastogenesis contributes to bone loss in the Costello syndrome Hras G12V mouse model. Front. Cell Dev. Biol. 2022, 10:1000575.
Caratti B, Fidan M, Caratti G, Breitenecker K, Engler M, Kazemitash N, Traut R, Wittig R, Casanova E, Ahmadian MR, Tuckermann JP#§, Moll HP#§, Cirstea IC#§. The glucocorticoid receptor associates with RAS protein complex to inhibit cell proliferation and tumor growth. Science Signaling 2022, 22;15(726):eabm4452. #§, equal contribution and joint coordination
Motta M*, Fidan M*, Bellacchio E, Pantaleoni F, Schneider-Heieck K, Coppola S, Borck G, Salviati L, Zenker M, Cirstea IC**, Tartaglia M**. Dominant Noonan syndrome-causing LZTR1 mutations specifically affect the Kelch domain substrate-recognition surface and enhance RAS-MAPK signaling. Hum. Mol. Genet. 2019, 28(6), 1007–1022. *, equal contribution; **, equal contribution and joint coordination
Cirstea IC, Gremer L, Dvorsky R, Zenker M, Ahmadian MR. Diverging gain-of-function mechanisms of two novel KRAS mutations associated with Noonan and Cardio-Facio-Cutaneous syndromes. Hum. Mol. Genet. 2013, 22(2):262-70.
Gremer L#, Merbitz-Zahradnik T#, Dvorsky R#, Cirstea IC#, Kratz CP, Zenker M, Wittinghofer A, Ahmadian MR. Germline KRAS mutations cause aberrant biochemical and physical properties leading to developmental disorders. Hum. Mutat. 2011, 32(1):33-43. #, equal contribution.
Cirstea IC, Kutsche K, Dvorsky R, Gremer L, Carta C, Horn D, Roberts AE, Lepri F, Merbitz-Zahradnik T, König R, Kratz CP, Pantaleoni F, Dentici ML, Joshi VA, Kucherlapati RS, Mazzanti L, Mundlos S, Patton MA, Silengo MC, Rossi C, Zampino G, Digilio C, Stuppia L, Seemanova E, Pennacchio LA, Gelb BD, Dallapiccola B, Wittinghofer A, Ahmadian MR, Tartaglia M, Zenker M. A restricted spectrum of NRAS mutations causes Noonan syndrome. Nat. Genet. 2010, 42(1):27-9.